Fear of the Invisible – The Groundbreaking Book and Investigation by Janine Roberts

August 23, 2008

The Nature of Viruses

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from the final chapter of Fear of the invisible..


The Nature of Viruses


There are some basic facts about viruses all biologists agree on.

Viruses have no metabolism so they cannot produce energy or eat. They have no nervous system, no sensory system, no intelligence that can facilitate any kind of invasion or hi-jacking of a cell a billion times larger.

But, the conventional theory of viral hijacking is that, after the short genetic code of a virus has been absorbed by a cell, the ‘viral genes’ absorbed start to ‘direct the production of proteins by the host cellular machinery.’ It is assumed they are able to force the host cell to do this, It is said they force the cell to assemble proteins into a shell or ‘capsid,’ to insert into this a clone of the original viral genetic code and then to launch it out of the cell by using the same machinery that the cell uses to harmlessly produce its own exosomes and other extra-cellular particles or vesicles.

But I had to ask, would cells give such minute and ‘dead’ messenger vesicle the extraordinary ability to pirate vastly larger and intelligent cells – including cells of the same organism?  This is the quandary we are left with if we agree that viruses are not alive and thus incapable of having a survival instinct.

But what if cells create viruses as weapons – against other cells?  If they do, then this would be remarkably suicidal as viruses usually pass from cell to cell within the same organism.

Such thoughts have left me deeply puzzled about the many pathogenic viruses reported to exist. I have severe doubts about some of these, particularly the poliovirus and HIV. I would have to look again at the evidence on other viruses.




Viruses are commonly blamed for illnesses that seem easily passed from one person to another. Bacteria may cause many of these  – but viruses are often blamed.  Our only medical weapons against them are said to be vaccination and powerful chemotherapy-type antiviral medicines designed to stop the cell from making viruses, rather than to attack the virus itself, for apparently it has proved too elusive a target.

But, why do cells make pathogenic viruses? Surely the reason for this has been established in numerous laboratory experiments? It is a doctrine in virology that cells make malignant viruses only after a disease virus arrives and infects them.

I had long presumed this must be so, but when I tried to analyse it, I had problems.  I found myself asking, since a virus cannot make a virus, surely the first viruses to cause an illness must have been made by an uninfected cell? 

I had earlier learnt how viruses did their damage. I had been told that they burst forth from infected cells, ‘exploding’ them. I was now surprised to discover that this is not so; that viruses are far too small, at one-billionth of the mass of a cell, to have this effect. 

Current courses on Medical Microbiology now teach, as mentioned briefly above,  that viruses kill or damage cells indirectly, by triggering cellular processes that do this damage. Professor Tritz blames allergic reactions.  ‘With animal viruses, cell lyses [death] is usually the result of one of four types of allergic reactions’ and  ‘allergy to viruses usually results in a very localized anaphylactic reaction.’ Alternatively, he suggests that the immune system sees the virus-producing cell as foreign and kills it. 

He also suggests that some illnesses are due to ‘toxic substances’ produced by cells because they are infected. ‘Virus-infected cells, at times, will produce compounds coded for by the host DNA, but which are not normally produced by the host. These are often cytotoxic at relatively high concentrations.’  Finally, some viruses might cause ‘structural alterations in the host cell’, affecting the chromosomes, moving the nucleus or creating bubble-like spaces, but so far I have been unable to locate experiments that prove viruses operating in isolation can cause such effects.

Another university course teaches, ‘virus infected cells may be recognized by the immune system, which leads to the destruction of the virus infected cells.’ 

From what they say, cell deaths are not directly due to viral infection. This perhaps makes sense. The virus is so minute compared to the cell – and our protective systems will destroy a very sick cell that does not self-destruct. Our cells often seem altruistically to decide to die when not needed, poisoned or otherwise diseased.

But on reflection, how can we prove cell’s illness is caused by the small viral genetic code it’s absorbed?  How can we be sure that a damaged cell is so solely because it is infected?  It may be naturally dying or poisoned.  It may even produce viral-like particles for waste disposal, or to attempt a cure or help protect other cells.

Also, if cell deaths in viral illnesses are mostly caused by our immune system, why do we have such deaths when the immune system is down, as surely it often is in such circumstances?

But nevertheless, viruses are encoded information, and since cells can make errors, I must conclude that they may sometimes wrongly encode the viruses they send out.  These in theory could misinform other cells, perhaps sometimes encouraging them to take courses of action that they would not take otherwise.  But as to how often the codes thus transported could lead to such effects, I had no idea.

I went to consult a standard textbook, ‘Introduction to Modern Virology’ by N. Dimmock and S. Primrose, published by Blackwell Scientific Publications.

On page 230 I found it surprisingly reported that, although people have presumed that flu is spread by coughing, ‘transmission experiments from people infected with a rhinovirus to susceptibles sitting opposite at a table proved singularly unsuccessful. Equally unsuccessful was the transmission of influenza from a naturally infected husband/wife to his/her spouse.’

Also on the same page it reported:  ‘it has been shown that recently bereaved people are susceptible to infectious diseases. Thus one’s resistance is influenced by one’s state of mind.’ It then went on to discuss winter life styles; such as living crowded in unventilated and over-heated rooms, all things it says might make us produce the symptoms of illness – and all things that make cells ill without any need of help from viruses.
It then concluded on page 212: ‘Evidently viruses do not kill cells by any one simple process and we are far from understanding the complex mechanisms involved …[it] seem more akin to death by slow starvation than acute poisoning. Lastly it is by no means clear what advantage accrues to the virus in killing its host cell. This situation may represent a poorly evolved virus-cell relationship or virus in the ‘wrong’ host cell.’

It thus seems that cells may be sick, poisoned, stressed or malnourished in some way before they show the symptoms of ‘viral infection.’ There is a considerable body of research that indicates cellular illness or malnourishment often precedes the production of viruses, rather than the converse. For example:  it is reported that deficiency in selenium, a metal our cells use as an antioxidant, can precede the symptoms of colds, flu and even AIDS. (There is also a strong co-relation between selenium levels in soils in African countries and the prevalence of AIDS symptoms. )

Dr Melinda Beck reported that selenium-deficient mouse cells show symptoms of illness and emit viruses.  She and her co-authors deduced from this that a lack of selenium made viruses dangerous – and consequently that these viruses made the cells ill.  But was this deduction soundly based?   Selenium is a component of glutathione peroxidase (GPX), an enzyme that protects cells from oxidative stress. Selenium-deficiency thus makes cells ill with oxidative stress without any need for a viral illness.  They consequently could produce viral-like particles as waste or for repair purposes.

Another research paper reported that, when cells are suffering from ‘oxidative DNA damage’ (such as from chemotherapy), then they are more likely to get hepatitis due to HCV viral infections. Again, what comes first?  The authors presume the virus must cause the illness – but surely the illness started with the earlier oxidative stress.

The first observation of retroviruses is credited to Peyton Rous. ‘It is generally accepted that Peyton Rous discovered retroviruses in 1911 when he induced malignancy in chickens by injections of cell-free filtrates obtained from a muscle tumour.’  But, when I went back to his records, I found that he also suggested that the cause of his chickens’ illness might be a chemical toxin in his filtrate! If retroviruses were indeed also present, might they have appeared as a defence against this toxin?

In earlier chapters we found that toxins, rather than viruses, are likely to be the primary causes of polio and AIDS – but what then about measles, mumps, flu and colds? 

I had long presumed the evidence for these illnesses being due solely to viral infection must be overwhelming – but I have found to my surprise that scientists have long known that the guaranteed way to make cells produce viruses in the laboratory, including flu and measles virus, is not primarily by getting them infected, but by exposing them to stress and toxins!

In 1928 the President of the Royal Society of Medicine’s Pathology Section, A. E. Boycott, in a report on the ‘nature of filterable viruses,’ stated that with toxins ‘we can with a considerable degree of certainty stimulate normal tissues to produce viruses.’ 

Then in 1963 the famous Sloan-Kettering Institute for Cancer Research reported that viruses multiplied after cells were exposed to ‘x-ray, ultraviolet light or certain mutagenic chemicals’ and that this exposure seemed to ‘alter the benign relationship’ that otherwise existed between cells and bacteria.

Then in the 1980s Robert Gallo reported that, when he added certain chemicals to cell cultures, these cells produced retroviruses. Gallo thus named these chemicals his viral ‘growth factor’ – and Montagnier at the Institut Pasteur used the same. If retroviruses were indeed thus produced, then surely this can be explained as a cellular response to stress from toxins?

In 2007 Dr Dominic Dwyer, a Senior Medical Virologist, formerly of the Institut Pasteur in Paris, testified that to persuade blood cells to produced HIV retroviruses, ‘we stimulate them with compounds such as PHA.’   He added; if we want to persuade cells to produce the flu virus ‘we use other things like tryspin.’ – thus that they expose cells to different chemicals to make them produce different viruses!  (Tryspin is destructive to proteins, and Phytohemagglutinin (PHA) is mitogenic. ) This surely suggests that virus production can be a cell’s response to being stressed and poisoned  – and that there might thus be no need for it to be infected beforehand?

Dr David Gordon, the Chair of the Clinical Drug Trials Committee at Finders University in Australia, testified, at the 2007 Parenzee trial in Australia, that there is no need to ‘purify a virus in order to identify it’.  He repeated emphatically: ‘No need to purify’ then rhetorically questioned: ‘Has any virus ever been purified?’  He explained: ‘The issues are exactly the same with any virus.’ He doubted if any virus was ever isolated from sick cells.  It seemed that a cellular illness was all the proof he needed to conclude that unseen viruses were present – no matter how artificial the laboratory circumstances or what chemicals were added.


So – viruses may not be the primary causes of illnesses – they might instead be caused by a cell being poisoned. Why  do our cells make them?  Could they be possibly a protective reacition ?


more on this in the book

 Medical Microbiology Fall 2000.  Tritz  Professor/Chairman Department Microbiology & Immunologyhttp://www.kcom.edu/faculty/chamberlain/Website/Lects/MECHANIS.HTM


  Burcher, Sam.  Selenium conquers AIDS?  Institute of Science in Society. http://www.i-sis.org.uk/AidsandSelenium.php

 Melinda A. Beck Antioxidants and Viral Infections: Host Immune Response and Viral Pathogenicity. Departments of Pediatrics and Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. April 27 2000 or 1999 issue of the FASEB Journal, a scientific journal published by the Federation of American Societies for Experimental Biology.

  Fabio Farinati et al. Oxidative DNA damage in circulating leukocytes occurse as an early event in chronic HCV infection.  Free Radical Biology and Medicine, December 1999. Pages 1284-1291.

 J. Exp. Med. vol. 13, no. 4, pp. 397-411 (April, 1911).


 Boycott AE. The transition form life to death; the nature of filterable viruses. Proc. Royal Soc. Med. 1928;22:55-69.

 Sloane-Kettering Institute for Cancer Research, Progress Report XV, Viruses and Cancer. January 1963

 Nucleic Acids Res. 1977 August; 4(8): 2713-2723.

 Nucleic Acids Res. 1977 August; 4(8): 2713-2723.


the hunt for the poliovirus – excerpt from Fear of the Invisible

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The Germ Theory of Disease


The Hunt for the Poliovirus


extracted from ‘Fear of the Invisible


‘At the heart of science lies discovery which involves a change in worldview. Discovery in science is possible only in societies which accord their citizens the freedom to pursue the truth where it may lead and which therefore have respect for different paths to that truth,’

John Polanyi, Canadian Nobel Laureate (Chemistry); Commencement Address, McGill University, Montreal, Canada, June 1990


The hunt for a virus that causes polio began in the first years of the 20th Century as an emergency response to the horrifying onset of major epidemics of paralytic polio in Sweden and the United States. It was guided by a new scientific hypothesis then gathering strength that we now know of as the Germ Theory of Disease.

These polio epidemics were new – and yet poliomyelitis, to give it its full name, was not a new disease. It had been around for centuries and was long associated with metalworking.  But the virus we now blame for polio is a common human gut virus with no obvious connection to metalworking. This virus is produced solely by human cells, and spreads from us to be common in soil. Human infants acquire lifelong immunity to it as soon as they go into the garden and put a grubby hand in their mouth, as stated in a paper published on the website of the Centers for Disease Control (CDC) in the US.

So – how did this virus come to cause these crippling and deadly epidemics? Sit back comfortably and read on, for this is also the story of the birth of modern virology and much of modern medicine. It took me some time to untangle it – but I think I can now explain it quite straightforwardly.


—————————– and the story continues…

We presume today that everyone knows that viruses cause major illnesses, but back in 1908, when the polio epidemics were starting to terrorise, viruses were not yet proved to cause illnesses; in fact they had not even been proved to exist! Initially it was speculated that viruses were smaller invisible versions of the barely visible single-celled bacteria that were already known to be able to reproduce and spread illnesses.

  Many medical theorists thought that epidemics were caused by minute filterable particles, like bacteria but so small that they could scarcely be seen. These were called viruses and an unknown one was suspected to cause polio…..

The scientists on the hunt conceived of viruses a priori as dangerous parasitic rivals to humans in the competition for life.  The electron microscope had not yet been invented, so for them these were invisible disease agents. Most viral ‘isolates’ were little more than filtered cell cultures in which viruses were presumed present. They were thus named ‘virus’ since this word means ‘poisonous liquid’ in Latin.

Ever since, viruses have been regarded with fear, as if intelligent nano-terrorists that ‘invade’ our cells, hijack them and outwit our defences. Viruses are feared as the ultimate mass destruction enemy, invisible agents able to kill millions in inevitable epidemics; mutant creatures that we must spend billions in fighting.

This is still the common view of viruses. ……… The virology specialists at that time, and ever since, have firmly dominated our major health institutions, such as the Centers for Disease Research, and persuasively held that epidemics must be caused by infectious agents, either bacteria or viruses.

I long believed the same. It seemed self-evident. In any case, as far as I then could judge, the very fact that polio vaccines now protect us from polio is sufficient proof that polio is caused by a virus……..

When I read the related research, I was surprised to discover how little we know of how the poliovirus causes polio. Professor Akio Nomoto of Tokyo University stated in 1996, ‘little is known about the mechanisms by which the poliovirus causes paralysis … it is not known how the virus moves into the blood from the primary multiplication site [the guts], how the virus invades the CNS [Central Nervous System] … Humans are simply lucky that the polio vaccines worked.’ He also noted the only way ‘polio can be shown to damage brain cells is to directly inject it across the barrier into monkey brains.’   This was a very major surprise; if this virus could not naturally get to these cells, how could it cause polio?

The World Health Organisation (WHO) credits the discovery of this virus, and of the infectious nature of polio, to a very famous experiment performed in Vienna in 1908 by Drs.  and Erwin Popper.


Koch and Pasteur inspired Landsteiner and Popper to begin their 1909 hunt for a virus causing polio.. As they couldn’t find a bacterium to blame for polio – they guessed there must exist minute invisible forms of bacteria able to pass through all available filters and still cause disease. They called these mini-bacteria ‘viruses.’  We now know that their filters would not have stopped many other particles, including DNA fragments, proteins, prions, toxins and much more. 

Landsteiner and Popper first looked for suitable animals to use and selected two monkeys that were made available by Sigmund Freud in Vienna, who had been testing their intelligence against that of humans. The experiment they then carried out is today celebrated by the World Health Organization, and by other authorities, as being the first to isolate the poliovirus and prove it causes polio.

It is still praised by our universities.  For example Leicester University on their website states the theory that polio is not caused by an infection ‘was finally dispelled by Landsteiner & Popper (1909), who showed that poliomyelitis was caused by a “filterable agent” – the first human disease to be recognized as having a viral cause.’ 

But when I read the details of their experiment, I was shocked by its crudeness and the questions it left unanswered. The experiment involved taking the spinal cord from a 9-year-old victim of polio, mincing this and mixing it with water. They then injected a cup of the resulting suspension of human cell debris, blood, DNA, RNA, proteins and enzymes – together with any viruses or toxins present – directly into the brains of these two living monkeys, as well as into other animals.

This toxic mix killed one of the monkeys immediately. The other was slowly paralysed – and later found to have ‘similar’ damage to its motor neurone cells as found in human polio cases. Landsteiner concluded the paralysis must be caused by an ‘invisible’ microbe present in the injected material. He wrote:  ‘The supposition is hence, that a so-called invisible virus or a virus belonging to the class of  causes the disease.’ (Protozoa are living single-celled entities, as are bacteria, and can reproduce independently. They are thus very different from what we call viruses.)

Landsteiner and Popper did not stop there. They wanted to prove their virus was infectious. They thus acquired more monkeys and tried to ‘transmit paralysis’ between them by grinding up the spinal cords from the sick monkeys and injecting these into the brains of other monkeys, as they had with the child’s spinal cords – a process that is still used in vaccine research and technically called ‘passaging.’ But, they were disappointed. They failed to pass on paralysis

The following year Simon Flexner and Paul Lewis of the illustrious Rockefeller Institute for Medical Research ‘proved’ a similarly made noxious soup was ‘infectious’ by succeeding where the above experiment had failed – by apparently passing paralysis from one monkey to another.   What they did was to similarly prepare a suspension of ground up human backbone and inject this into the living brain of a monkey. They then extracted some fluid from its brain, injected this into another monkey’s brain, and so on through a series of monkeys, but this time succeeding in paralysing all of them in the process.

Flexner and Lewis recorded their experiment in the pages of the Journal of the American Medical Association. Their conclusion was: ‘We failed utterly to discover bacteria, either in film preparations or in cultures, that could account for the disease,’ They then went on to say the cause must then be the mysterious virus:  ‘The infecting agent of epidemic poliomyelitis belongs to the class of the minute and filterable viruses that have not thus far been demonstrated with certainty under the microscope.’ Toxic causes were not even considered – let alone the multitude of other things that could well have been in this toxic stew injected directly into the monkeys’ brains, thus completely bypassing their immune systems.

Such a soup cannot possibly be considered an  ‘isolate’ of the tiny organism we now call a virus – despite this now being widely claimed. It also proved strangely non-infectious for a virus, for Flexner and Lewis found that the monkeys were not paralysed when made to drink it or when one of their limbs was injected with it, nor did they infect other monkeys. It had to be injected into their brains to have any effect.

The procedures of Flexner and Lewis were just as dubious as their conclusions. They took no account of the contaminants in their mashed-up soup and presumed what happened in monkeys would be replicated in humans. Their experiment thus shed no light on what element had paralysed the monkeys, and for that matter, what had paralysed the children with polio.

Yet these experiments are today celebrated in virology as of great historical importance, as being the first time a virus was proved to cause a major epidemic.   But – how could these experiments be so celebrated? How could a scientist credibly claim that injecting cellular debris into the skull of a monkey proves a virus to cause polio?

The more I read of what are supposed to be the victories of polio research, the more I have been, quite frankly, appalled. During the 1920s and 1930s all kinds of biological materials-spinal cord, brain, faecal matter, even flies-were ground up and injected into monkey brains to induce paralysis, causing great harm to many animals  – all in the hope that such experiments would explain why humans were getting summer polio.

The method they used to exclude bacteria from their injected sample of backbone was also quite extraordinary. They put some of the backbone suspension into a dish and watched to see what happened.  They reported: ‘If there was no [bacterial] growth after approximately 22 hours of incubation at 37 C., the specimen was considered suitable for inoculation into monkeys. This was not a sterility test, since growth would usually occur on longer incubation; it was rather an indication of the amount of bacterial contamination in the specimen.’ Slow growing bacteria were thus deliberately not removed – and no toxin was looked for – yet they knew these might well be present.

From all I read, I was forced to conclude that these ‘scientists’ shared a doctrinal conviction that the cause of polio must be a particular virus and could be nothing else. They routinely described as ‘isolated virus’ what was nothing much more than fluid from a cell culture contaminated with many diverse particles and possibly toxins. What else but an irrational belief in a theory could so blind these scientists?

Yet, for a long time they admitted that they could not actually locate a particular particle within these various ground up suspensions called ‘viruses’  – let alone separate it out so it could be identified. Their practical concept of a virus thus seemed not to differ to any significant degree from the cowpox pus that Jenner had first named as a virus over a hundred years earlier.

The search for the poliovirus led to the invention of the electron microscope in 1932 by Ruska and Knoll, but the epidemics continued unchecked. This made the public extremely impatient with the health authorities, for all they had been told during the first half of the 20th century was that a mysterious invisible virus caused polio and was public enemy Number One – without it ever being identified.

It was not only polio research that was so blighted.  Dr Max Theiler of the Rockefeller Institute claimed he had invented a vaccine against yellow fever. He had made it by taking serum samples from sick patients and ‘passaging’ these repeatedly by growing them in mice tissues.  He took fluid from the final mouse in the series and injected this into fertilized chicken eggs. After a week of incubation, the chick-embryos were removed from the eggs and finely minced. Human blood serum was then added to ‘stabilize’ the viruses, although this may give the bird and mouse viruses the chance to mutate into forms that might infect humans. The resulting fluid was his yellow fever vaccine. In 1938 more than one million Brazilians were inoculated with this vaccine before it was discovered that it was contaminated with hepatitis B. 

Another example: Harris in 1913 injected filtered tissue material from pellagra victims into monkeys and observed a similar disease developing in these animals. He concluded a virus must be present and be the cause of pellagra.  But it was then discovered that this disease is not caused by a virus but by vitamin deficiency. Dr. R. Scobey scathingly commented in 1952: ‘It is obvious that if the investigations of pellagra had been restricted to the virus theory, it would still be a mystery.’

It was only in the late 1940s that the scientists researching polio came to identify a particular virus with polio.  It was through what is now another famous experiment.  In 1948 Gilbert Dalldorf and Grace M. Sickles of the New York State Department of Health claimed to have ‘isolated’ in the faeces of paralyzed children an ‘unidentified, filterable agent’ or ‘virus’ that might be the cause of polio.

They had done so by diluting the excrement of polio-victims.  They said they took a ‘20% faecal suspension, prepared by ether treatment and centrifugation.’ (Ether to kill bacteria and centrifugation to remove large particles.) This they had injected ‘intracerebrally into mice’- meaning into the living brains of mice. The result was ‘suckling mice, 3-7 days of age, became paralyzed…’

So what had they proved with this experiment? Surely, only that paralysis could be induced in young mice by injecting diseased human excrement into their young brains?  I was utterly shocked that serious scientists could get away with describing this as the successful ‘isolation’ of a virus that they had thus proved to cause polio in humans.

The highly respected bacteriologist Claus Jungeblut critically stated that such ‘viral isolates,’ including those developed by Salk and other vaccine scientists, had not been proved to cause polio – as they had not been shown to give monkeys the disease found in human cases of infantile paralysis – and thus had failed to meet the Koch Postulates.

In fact quite the contrary had been demonstrated. Jungeblut said the virus would be so changed or mutated by the way these vaccine scientists passaged it through monkey cells that it would be quite unlike the wild virus by the time it was used for a vaccine.  He concluded: ‘The highly specialized … virus which has been maintained in the past by intra-cerebral passage in rhesus monkeys is more likely a laboratory artefact than the agent which causes the natural disease in man.’

It also might not be the only agent at work. Daldorf and Sickle thought at one point that they had detected an agent at work alongside the ‘poliovirus,’ helping to cause polio. ‘The patients we studied may possibly have been coincidentally infected with the new agent and classical poliomyelitis virus.’  They tried to test the putative ‘new agent’ but it was ‘not successful in [causing disease in] the rhesus monkey.’

Their experiment was in 1949. It was immediately used as the scientific basis for the development of the polio vaccines. I was utterly horrified to learn that this noxious faeces-derived suspension they called a ‘poliovirus’ was soon being experimented with as a ‘vaccine seed’ to use for our polio vaccines. All this was for me a rude awakening. I never expected to read such crude science.  But, I clung to a last hope  – surely it could not have been dangerous, for if it were then surely many thousands of vaccinated children would be falling ill? Somehow or other, it must have been purified?

Up until around the time of Daldorf and Sickle’s experiment, scientists had logically sought to find the suspect poliovirus in the diseased spinal cords and nerves of polio victims, where it should be found if it caused the illness. That was why they had focused on similar nerve tissue in monkeys. But by 1945 they had searched for over 30 years – and no virus had yet been identified in these tissues as responsible for this damage.

Monkeys were expensive to acquire, but nevertheless many thousands were bought and ‘sacrificed’ in this hunt. Sabin exposed hundreds of monkeys to cellular material from his polio patients and then watched the monkeys for a month to see if weakness or paralysis developed. If it did, then he performed autopsies to see if the monkeys had suffered the damage to the spinal cord found in human polio victims.  But for him these studies failed, for he could not find in the damaged tissues the virus he was convinced must cause this damage.

Prior to Daldorf and Sickle’s experiment many scientists had similarly hopefully named their filtered fluid samples from monkey brains as the ‘poliovirus’ – but in each case had failed to prove it caused polio.  But, if they had succeeded, then growing enough of this to make the vaccine would have proved extremely expensive. The National Foundation for Infantile Paralysis estimated in 1948 that to grow enough poliovirus to inoculate all Americans would need the ‘sacrifice’ of 50,000 monkeys.

Thus Daldorf and Sickle’s ‘findings’ were most welcome to Sabin and other polio vaccine developers, No longer would they need to try to find the poliovirus in expensive monkeys.  No longer would they have to search for it in the nerve cells it reputedly damaged, for Daldorf and Sickle had found it in easily procured human excrement. Under the electron microscope, a small ball-like particle was located in diluted excrement and named as the poliovirus. It was logically classified as ‘enterovirus,’ a gut virus  – not a nerve virus at all, but in their elation, they left aside the issue of how a virus in the gut could cause polio in backbone and brain nerve tissues.

This tiny particle, some 24-30 nm (thousand millionths of a meter) in width, isolated from excrement, thus became the basis of our polio vaccine.  Dr Salk developed the first commercial polio vaccine with virus found in ‘the pooled faeces of three healthy children in Cleveland.’ It was not found in the victims of polio. 

 See Dr. John H. Lienhard of the University of Houston, author of Polio and Clean Water on the CDC website


  ‘Molecular Mechanism of Poliovirus Replication – Control of Poliomyelitis’ Akio Nomoto (Professor, The Institute of Medical Science, The University of Tokyo, Japan) 1996

  The Journal of Immunology, vol.140, p.564



   The 1853 Compulsory Vaccination Act

 The Case Against Vaccination. AN ADDRESS By WALTER HADWEN
J.P., M.D., L.R.C.P., M.R.C.S., L.S.A., Etc
(Gold Medalist in Medicine and in Surgery) At GODDARD’S ASSEMBLY ROOMS, GLOUCESTER. On Saturday, January 25th, 1896
(During the Gloucester Smallpox Epidemic)

 . http://www.thedorsetpage.com/History/Smallpox/smallpox.htm

   The Lancet 2002; 360:93 http://www.thelancet.com/journals/lancet/article/PIIS0140673602093637/fulltext

  As above.

 Bechamp wrote thus in 1869 of their role in disease:  ‘In typhoid fever, gangrene and anthrax, the existence has been found of bacteria in the tissues and blood, and one was very much disposed to take them for granted as cases of ordinary parasitism. It is evident, after what we have said, that instead of maintaining that the affection has had as its origin and cause the introduction into the organism of foreign germs with their consequent action, one should affirm that one only has to deal with an alteration of the function of microzymas.’

 Andrew Mendelsohn, Princeton dissertation. http://www3.imperial.ac.uk/historyofscience/aboutthecentre/staff/drandrewmendelsohn

 On the Anthrax Inoculation [1872] by Robert Koch from Professor K. Codell’s book ‘Essays of Robert Koch’, Greenwood Press, N.Y., 1987.

 Evidence given by Sir John Simon, chief medical officer to the Privy Council,

 Preface to Brock’s Robert Koch: A Life in Medicine and Bacteriology  by James Strick, Program in Biology and Society,  Arizona State University, Tempe, AZ 85287-1501

 JSTOR Isis. Vol 86 no 2 (june 1995) pp 268-277. Typhoid Mary stirkes back by Andrew Mendelsohn.

  Cited above.

 Chicago Tribune, November 23, 1893 

 http://www-micro.msb.le.ac.uk/109/introduction.html Leicester University – notes for undergraduates reading microbiology. 

 Landsteiner K, Popper E. Übertragung der poliomyelitis acuta auf affen. Z Immunitätsforsch 1909;2:377-390.

 S Flexner and PA Lewis; The Journal of the American Medical Association; 33: 639; 13 November 1909

 S Flexner; [Trans M Rec]; 78:924-926; 19 November 1910. Also R Scobey; ‘Is the public health law responsible for the poliomyelitis mystery?’ Archive Of Pediatrics; May 1951

 F.B. Gordon and colleagues in the Journal of Infectious Diseases,

 Personal communication in 2007 to author from Professor Etienne De Harven.

 Polio Vaccines and the Origin of AIDS   B. F. Elswood and R. B. Strickler

Medical Hypotheses, vol. 42, 1994, pp. 347-354

 G Dalldorf and GM Sickles; ‘An unidentified, filterable agent isolated from the faeces of children with paralysis’; Science; 108: 61; 1948

 CW Jungeblut; Journal of Pediatrics; 37: 109; July 1950. R Scobey; Archives of Pediatrics; April 1952

 A.B. Sabin, A.B. & L. Boulger, History of Sabin Attenuated Poliovirus Oral Live Vaccine Strains. 1 J. BIOL. STAND. 115, 115-18 (1973).

July 13, 2008

Fear of the Invisible – Book Release

Filed under: Uncategorized — janineroberts @ 12:42 pm


How scared should we be
of viruses and vaccines,


Fear of the Invisible
by Janine Roberts
isbn 0955917727, amazon.com

An Investigative Journey into a reckless and contaminated Medical Industry
This book takes its readers on a journey into the very heart of the hunt for viruses – to the key experiments performed to prove that these invisibly small particles cause diseases that often were previously blamed on toxins or bacteria. It sheds light on the extraordinary assumptions underlying much of this research into viruses – and the resulting vaccines and antiviral medicines.

The author, an investigative journalist who researched and produced investigative films for the BBC, American and Australian television, was asked by parents with children severely ill after vaccination to discover if the medical authorities were hiding anything from them. She agreed, but had no idea how long this search would take or how it would change her ideas. She expected at best to uncover a small degree of contamination.

On the ensuing decade-long journey of discovery, she found top government scientists report alarmingly, at meetings between scientists, that it is impossible to purify vaccines. They stated that the childhood vaccines of today are contaminated with viruses from chickens, humans and monkeys, with RNA and DNA fragments, with “cellular degradation products,” and possibly “oncogenes and prions.”

They say they dare not tell the pubic about all this contamination – as they might demand a withdrawal of the vaccines. Thus the public is not told despite all the consequences of such contamination for long-term public health. A US court decision in 2008 has linked autism with vaccine contamination. The author cites her sources by name – and gives references and Internet links where they are available.

There is much research here that has not been reported elsewhere. She reveals, for example, that the World Health Organization (WHO) knows the MMR vaccine is contaminated with chicken leukosis virus, yet has decided not to tell the public and to continue to make the vaccine with eggs from contaminated chickens. She doubts the accuracy of their research, as it is based on discovering an enzyme, RT, not a virus, but they believe it is very dangerous to chickens and potentially to children. They stay silent because to confess this would reveal that they cannot purify the vaccines given to our children.

She reports US biowarfare researchers tried to create new agents to destroy human immune systems – and reported working on a bacterium to make it a hospital superbug. Did they manage to create HIV? She thought it unlikely as military personnel were not AIDS first victims. Besides there was a more likely alternative. A senior professor told her the vaccine program was so contaminated and chimps were used in vaccine manufacturing so widely, that HIV could easily have spread in a vaccine without any need for military intervention. She then set out to find why HIV spread so far and so fast. Was it in a vaccine? She needed to know more about HIV so went to the foundation research widely held today to have found this virus and proved it caused AIDS.

She was then rocked to discover that this key HIV research was investigated for scientific fraud by powerful US scientific institutions and by Congress. Why is this not widely known? These reported major errors in this research, with some errors so serious that the inquiries said they made it impossible to repeat these experiments and verify them! She reveals the evidence unearthed – reproducing key documents so the reader can assess them for themselves. This is explosive material.

She then finds the faults in researching HIV apply also to other viruses. She goes to the key experiments and can find none in which pure samples of viruses were produced and proved to cause particular human diseases. If they cannot purify viruses for use in vaccines, they cannot produce the pure cultures needed to link with certitude viruses with diseases.

The book discusses in detail the attack on the Perth group in an Australian court in 2007. During this many HIV experts said again and again – ‘but we don’t isolate other viruses. `it is not only HIV that we do not isolate.’ They described how they produced the flu and measles virus. The author shows how measles virus is produced according to the latest CDC guidelines. it is as strange as anything done with HIV. At no point is the virus actually detected and identified.

A major part of the book takes its readers on a journey through various aspects of HIV theory, such as sexual transmission, the different clinical definitions of AIDS, why AIDS is said to be caused by HIV and at the same time is said to happen in the absence of HIV, and why the HIV test picks up on different diseases in the West and in Africa.

In the final part of this book the author reports recent research that is revolutionizing biology and offering much hope for the future. These new developments shed new light on the relationships between our cells and viruses. They are not necessarily enemies. Readers may find these new developments will radically change the ideas they have held about viruses all their lives.

The preface is contributed by Dr Roberto Giraldo. The book has hundreds of scientific references, a scientific glossary and an index.

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